We have shown that both excitatory (glutamatergic) and inhibitory (GABAergic) cells in the inferior colliculus (IC) project to and synapse on cells in the auditory thalamus (MGB). Our long-term objective is to understand the role of these excitatory and inhibitory IC inputs in shaping the responses of cells in the MGB. The sensory thalamus was once considered to be a simple relay center whose cells received ascending sensory information and passively sent it on to the cortex. Over the past 3 decades it has become apparent that this is not the case and that thalamic cells can function in two different response modes, "burst" and "tonic" which depend on the activation or inactivation of a voltage sensitive calcium conductance. Depending upon which mode the cell is in drastically alters their spike response to ascending excitatory synaptic messages and thus changes their input to the cortex in response to sensory stimuli (see Sherman, '01). In addition, the synchronized response of populations of thalamic cells while in the burst mode are believed to be responsible for the EEG oscillations seen during slow wave sleep and during some types of generalized epileptic seizures (see McCormick and Bal, '97). Recent evidence primarily from our lab has indicated that an added level of complexity is found in the auditory thalamus. Here 1) in contrast to other sensory thalamic nuclei, the ascending synaptic information is in the form of both excitation and inhibition 2) this ascending sensory input may be influencing auditory thalamic cells that do not necessarily display the two different response modes and 3) this ascending sensory input from the IC to some cells in the MGB may show synaptic plasticity. Thus, models of thalamic function that have been created using other sensory systems may not be applicable to the auditory thalamus. In order to better understand the similarities and/or differences in auditory thalamic processing of sensory information it is important to determine 1) how and when the excitatory and inhibitory IC inputs are active and thus influencing thalamic neurons 2) whether these inputs are influencing cells that can respond either in one mode or two and 3) whether stimulation of the collicular inputs can generate synaptic plasticity (LTP) in certain MGB cells and what mechanism of potentiation is involved. The proposed experiments will help to answer these questions.